The sodium-potassium stimulated adenosinetriphosphatase (Na - K- ATPase) in the vascular smooth muscle cell (VSMC) plays an important role in regulation of the vascular tone. Studies within the last decade have suggested that the activity of this enzyme (or its physiological analogue, the Na - K - pump) may be altered in essential hypertension in man and models of hypertension in experimental animals. We have developed techniques that make it possible to assay this enzyme in in-vitro preparations of VSMC's. In the present study we will examine the hypothesis that the activity of this enzyme in VSMC's derived from rat species with genetic predisposition to hypertension is different from that of VSMC's obtained from their normotensive counterparts. Primary explants of vascular tissue will be obtained from various arteries of the Okamoto strain of spontaneously hypertensive (SHR) rats, Dahl strains of salt sensitive (DS) and salt resistant (DR) rats, as well as their appropriate controls. The vascular explants will be processed for in-vitro propagation and enrichment of VSMC's. We will examine the specific activity of Na - K - ATPase, its enzyme kinetics, and (3H) ouabain binding sites in the VSMC"s under a) basal conditions, b) following chronic alterations in dietary sodium or potassium, c) chronic changes in sodium and potassium concentrations in the growing media that will be used to propagate the vsmc's and d) influence of agents and hormones with potential capacity to alter the vascular tone. The present study provides a new approach toward assessing the role of both intrinsic elements in VSMC's and extracellular factors that may contribute to an abnormal activity of Na - K - ATPase in VSMC's in hypertension of gentic origins.